Document Detail


Pan-CC chemokine neutralization restricts splenocyte egress and reduces inflammation in a model of arthritis.
MedLine Citation:
PMID:  20644170     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chemokines are key regulators of leukocyte trafficking and play a crucial role under homeostatic and inflammatory conditions. Because chemokines are involved in multiple pathologies, they represent an attractive class of therapeutic targets. However, because of the redundancy of this system, neutralizing a single chemokine may be insufficient to achieve therapeutic benefit. Our strategy was to use a Fc-fusion recombinant protein form of the poxvirus-derived viral CC chemokine inhibitor protein (vCCI-Fc) that has the ability to specifically bind to multiple CC chemokines and neutralize their activity. In this study, we demonstrate first that, in vivo, vCCI-Fc prevents CC chemokine-dependent migration of macrophages into inflamed tissue of carageenan-challenged mice. We next studied this effect of inhibiting CC chemokine activity in a model more relevant to human disease, collagen-induced arthritis. Mice receiving vCCI-Fc revealed a striking retention of splenocytes, including activated and IFN-gamma-secreting CD4(+) and CD8(+) T cells, that was associated with a concomitant decrease of cells in the draining lymph nodes. These phenomena resulted in a significant decrease in the incidence of disease and a reduction in clinical score, joint inflammation, and cartilage destruction as compared with mice receiving isotype control. Taken together, these results define a role for CC chemokines in the control of disease, as interfering with their function leads to a previously unappreciated role of controlling inflammatory cell trafficking in and out of secondary lymphoid organs.
Authors:
Vanessa Buatois; Séverine Fagète; Giovanni Magistrelli; Laurence Chatel; Nicolas Fischer; Marie H Kosco-Vilbois; Walter G Ferlin
Publication Detail:
Type:  Journal Article     Date:  2010-07-19
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-08-05     Completed Date:  2010-09-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2544-54     Citation Subset:  AIM; IM    
Affiliation:
NovImmune SA, Geneva, Switzerland.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arthritis, Experimental / immunology*,  prevention & control
Cell Line, Tumor
Cell Movement / drug effects,  immunology
Chemokines, CC / antagonists & inhibitors,  immunology*,  metabolism
Female
Flow Cytometry
Humans
Immunoglobulin Fc Fragments / genetics,  metabolism
Inflammation / immunology*,  prevention & control
Interferon-gamma / immunology,  metabolism
Lymphocyte Count
Macrophages / cytology,  immunology,  metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Inbred DBA
Protein Binding
Recombinant Fusion Proteins / immunology*,  metabolism,  pharmacology
Spleen / cytology,  immunology,  metabolism
T-Lymphocytes / drug effects,  immunology,  metabolism
Vaccinia virus / genetics,  metabolism
Viral Proteins / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Chemokines, CC; 0/Immunoglobulin Fc Fragments; 0/Recombinant Fusion Proteins; 0/Viral Proteins; 82115-62-6/Interferon-gamma

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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